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. 2018 Jun 7;4(2):75-94.
doi: 10.1016/j.cdtm.2018.03.003. eCollection 2018 Jun.

Air pollutants and early origins of respiratory diseases

Affiliations

Air pollutants and early origins of respiratory diseases

Dasom Kim et al. Chronic Dis Transl Med. .

Abstract

Air pollution is a global health threat and causes millions of human deaths annually. The late onset of respiratory diseases in children and adults due to prenatal or perinatal exposure to air pollutants is emerging as a critical concern in human health. Pregnancy and fetal development stages are highly susceptible to environmental exposure and tend to develop a long-term impact in later life. In this review, we briefly glance at the direct impact of outdoor and indoor air pollutants on lung diseases and pregnancy disorders. We further focus on lung complications in later life with early exposure to air pollutants. Epidemiological evidence is provided to show the association of prenatal or perinatal exposure to air pollutants with various adverse birth outcomes, such as preterm birth, lower birth weight, and lung developmental defects, which further associate with respiratory diseases and reduced lung function in children and adults. Mechanistic evidence is also discussed to support that air pollutants impact various cellular and molecular targets at early life, which link to the pathogenesis and altered immune responses related to abnormal respiratory functions and lung diseases in later life.

Keywords: Air pollutants; Early disease origin; Particulate matter; Polycyclic aromatic hydrocarbon; Respiratory diseases.

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Figures

Fig. 1
Fig. 1
Schematic demonstration of air pollutants: the vapor form (A) of organic air pollutants exemplified with the structure of benzo [a]pyrene (B) and the particulate form (diesel exhaust particles or particulate matters) of air pollutants (C).
Fig. 2
Fig. 2
Schematic demonstration of prenatal origin of respiratory diseases. PAH: polycyclic aromatic hydrocarbon; FEV1: forced expiratory volume in 1 second; COPD: chronic obstructive pulmonary disease. DEP: diesel exhaust particle; IL: interleukin; Th2: type II helper T cells; IgE: immunoglobulin E; NK: natural killer cells.

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